A randomised, double blind, placebo controlled trial with vitamin D<sub>3</sub>as an add on treatment to interferon β-1b in patients with multiple sclerosis

Soilu‐Hänninen, Merja; Åivo, Julia; Lindström, Britt Marie; Elovaara, Irina; Sumelahti, Marja Liisa; Färkkilä, Markus; Tienari, Pentti J.; Atula, Sari; Sarasoja, Taneli; Herrala, Lauri; Keskinarkaus, Irma; Krüger, Johanna; Kallio, Timo; Rocca, Maria A.; Filippi, Massimo

doi:10.1136/jnnp-2011-301876

Cited by 254 publications

(219 citation statements)

References 35 publications

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“…That is, vitamin D may decrease inflammation Modern studies of the clinical use of physiological doses of vitamin D are relatively rare (around 5,000 IU/day, see above). At least one RCT of physiological doses shows vitamin D may be clinically helpful as add on treatment in multiple sclerosis, 89 active tuberculosis, 90 rheumatoid arthritis, 91 and lupus, 92 all inflammatory diseases. All clinical treatments decisions are based on a risk/benefit analysis.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D and inflammation

Cannell¹,

Grant

Holick

2014

Dermato-Endocrinology

177

131

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Abbreviations: CRP, C-reactive protein; CXCL9, CXC chemokine ligand 9; E-selectin, ESR, erythrocyte sedimentation rate, F1C2, prothrombin fragment 1C2; IFG, impaired fasting glucose; IL, interleukin; MCP-1, monocyte chemoattractant protein-1; NGAL, neutrophil gelatinase-associated lipocalin; NGT, normal glucose tolerance; ns, not stated; PAI-1, plasminogen activator inhibitor-1; sICAM-1, soluble intracellular adhesion molecule-1; sTNF-R2, soluble tumor necrosis factor a receptor type 2; TAT, thrombin antithrombin complex; TGF-b, transforming growth factor-b; TNF-a, tumor necrosis factor-a Seventeen found significantly reduced inflammatory markers, 19 did not, one was mixed and one showed adverse results. With few exceptions, studies in normal subjects, obesity, type 2 diabetics, and stable cardiovascular disease did not find significant beneficial effects. However, we found that 6 out of 7 RCTS of vitamin D 3 in highly inflammatory conditions (acute infantile congestive heart failure, multiple sclerosis, inflammatory bowel disease, cystic fibrosis, SLE, active TB and evolving myocardial infarction) found significant reductions. We found baseline and final 25(OH)D predicted RCTs with significant reduction in inflammatory markers. Vitamin D tends to modestly lower markers of inflammation in highly inflammatory conditions, when baseline 25(OH)D levels were low and when achieved 25(OH)D levels were higher. Future inquiries should: recruit subjects with low baseline 25(OH)D levels, subjects with elevated markers of inflammation, subjects with inflammatory conditions, achieve adequate final 25(OH)D levels, and use physiological doses of vitamin D. We attempted to identify all extant randomized controlled trials (RCTs) of vitamin D that used inflammatory markers as primary or secondary endpoints.

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Section: Discussionmentioning

confidence: 99%

Vitamin D and inflammation

Cannell¹,

Grant

Holick

2014

Dermato-Endocrinology

177

131

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“…Moreover, any intervention study of vitamin D in RRMS will have to be an add-on to a conventional immunomodulatory drug with a proven effect on the outcome measures that are relevant for vitamin D. A brief look at observational studies in patients treated with interferons underscores the need for large sample sizes. Thus, one study of 1482 RRMS patients followed for 2 years found lower rates of new MRI activity with increasing 25(OH)D levels, with the lowest rate of new lesions (relative risk = 0.53) for those with 25(OH)D exceeding 100 nmol/l [15]. In another study 25(OH)D was associated with time to relapse or MRI activity in the 97 patients receiving interferon-beta (hazard ratio = 0.58), but not for those 151 receiving glatiramer acetate (hazard ratio = 0.89) [16].…”

Section: Can Vitamin D Reduce Inflammation In Relapsing-remitting Mulmentioning

confidence: 99%

Can vitamin D reduce inflammation in relapsing-remitting multiple sclerosis?

Holmøy

Torkildsen

2016

Expert Review of Neurotherapeutics

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“…Specific deletion of the GM‐CSF receptor on these monocytes, but not on DC, diminished disease severity 39. Multiple sclerosis is associated with VD3 deficiency; its murine model experimental autoimmune encephalomyelitis, and possibly also multiple sclerosis itself, is ameliorated by VD3 supplementation 40, 41. Hence, we speculate that, paralleling the in vitro studies of moDC outlined above, high VD3 conditions in vivo may redirect monocyte differentiation into tolerogenic versus inflammatory DC and contribute to the potential therapeutic effects of such supplementation.…”

Section: Potential Relevance Of Culture Models To Inflammatory (Monocmentioning

confidence: 99%

Vitamin D immunoregulation through dendritic cells

2016

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SummaryVitamin D (VD3) has been linked to immunological processes, and its supplementation may have a role in treatment or prevention of diseases with underlying autoimmune or pro‐inflammatory states. As initiators of the immune responses, dendritic cells (DC) are a potential target of VD3 to dampen autoimmunity and inflammation, but the role of DC in VD3‐mediated immunomodulation in vivo is not understood. In addition to being targets of VD3, DC can provide a local source of bioactive VD3 for regulation of T‐cell responses. Here we review existing studies that describe the tolerogenic potential of VD3 on DC, and discuss them in the context of current understanding of DC development and function. We speculate on mechanisms that might account for the potent but poorly understood tolerogenic activities of VD3 and the role of DC as both targets and sources of this hormone.

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A randomised, double blind, placebo controlled trial with vitamin D₃as an add on treatment to interferon β-1b in patients with multiple sclerosis

Abstract: EudraCT number 2007-001958-99 and ClinicalTrialsGov number NCT01339676.

Cited by 254 publications

References 35 publications

Vitamin D and inflammation

Vitamin D and inflammation

Can vitamin D reduce inflammation in relapsing-remitting multiple sclerosis?

Vitamin D immunoregulation through dendritic cells

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A randomised, double blind, placebo controlled trial with vitamin D3as an add on treatment to interferon β-1b in patients with multiple sclerosis

Abstract: EudraCT number 2007-001958-99 and ClinicalTrialsGov number NCT01339676.

Cited by 254 publications

References 35 publications

Vitamin D and inflammation

Vitamin D and inflammation

Can vitamin D reduce inflammation in relapsing-remitting multiple sclerosis?

Vitamin D immunoregulation through dendritic cells

Contact Info

Product

Resources

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A randomised, double blind, placebo controlled trial with vitamin D₃as an add on treatment to interferon β-1b in patients with multiple sclerosis